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Biomedical subjects

E Masini

Publications and source records attributed to E Masini.

At least 145 records · Page 8Linked to original sources
PubMed1980

Inhibition of cholinergic histamine release in rat mast cells.

Adrenaline inhibits the acetylcholine-evoked histamine release from isolated purified rat mast cells, in a dose-dependent fashion. The inhibitory effect of adrenaline is reversed by preincubating the cells with a beta-blocker, aprenolol, but not by preincubating them with an alpha-blocker, phentolamine. These results were confirmed by observations using an electron microscope and they suggest that adrenaline inhibits the cholinergic histamine release from rat mast cells acting upoon beta-receptors.

Acetylcholine↗
PubMed1980

Characteristics of histamine release evoked by acetylcholine in isolated rat mast cells.

1. Histamine secretion from rat mast cells occurs in the presence of nanomolar concentrations of acetylcholine. 2. Intact glycolytic and oxidative metabolism is required for the acetylcholine-induced histamine secretion. Removal of extracellular glucose, hypoxia, cyanide and monoiodoacetate almost completely inhibit the secretion. 3. The secretion of histamine is dependent on the extracellular H ion concentration and is blocked when the cells are exposed to Na-deficient media. 4. The order of potency of cholinrgic agonists in evoking the secretion of histamine is oxotremorine > acetylcholine > choline > carbamycholine > nicotine. 5. Atropine competitively blocks the acetylcholine-induced histamine secretion, indicating the presence of cholinergic muscarinic receptors on mast cells. 6. Dibutyryl cyclic AMP and adrenaline inhibit the acetylcholine-induced histamine secretion, indicating a regulatory function afforded by cyclic nucleotides in the cholinergic histamine release.

Acetylcholine↗
PubMed1978

Modulation of the spontaneous histamine release by adrenergic and cholinergic drugs.

Experiments have been reported on the possible modulation of the spontaneous histamine release by adrenergic and cholinergic drugs. Adrenergic drugs increase the spontaneous histamine release in vivo, and in neoplastic mast cells, in vitro. The mechanism of histamine release appears to be dependent upon the activation of alpha-adrenoceptors. Cholinergic drugs activate the release of histamine in many secretory processes in vivo; in vitro, acetylcholine is one of the most powerful histamine releasers in isolated purified rat mast cells. The release of histamine evoked by acetylcholine in rat mast cells is a calcium-requiring, temperature-dependent exocytosis. The physiological relationship of the sympathetic, parasympathetic and histamine-containing cells are discussed.

Animals↗
PubMed1977

The influence of catecholamines and serotonin on histamine uptake and metabolism by guinea pig atrium.

The influence of serotonin and catecholamines on the uptake and metabolism of 14C-histamine by isolated guinea pig atrium has been investigated. Epinephrine, norepinephrine and serotonin were found to reduce the histamine uptake and the formation of methylhistamine, in a dose-dependent fashion. The order of potency was epinephrine greater than norepinephrine greater than serotonin. Aliphatic diamines, such as spermine, do not affect the accumulation and metabolism of histamine. It is suggested that serotonin and catecholamines, may enhance histamine responses by decreasing the uptake and metabolism of this amine.

Animals↗
PubMed1977

The modulation of histamine release by alpha-adrenoceptors: evidences in murine neoplastic mast cells.

Murine neoplastic mast cells which have been loaded with exogenous labelled histamine, released 14C-histamine when exposed to increasing concentrations of phenylephrine and noradrenaline. Adrenaline was only slightly effective, while isoprenaline and dibutyryl-cyclic-AMP were fully inactive. The release of histamine evoked by alpha-adrenergic agonists was antagonized by phentolamine, and left unchanged by practolol and cocaine. It is concluded that alpha-adrenoceptors may be valuable in evoking histamine release by murine neoplastic mast cells.

Animals↗
PubMed1976

A trend in the therapy of Amanita phalloides poisoning.

Recent experimental evidences have been produced on the protection afforded by penicillin G in rats poisoned by Amanita phalloides extracts. A therapeutic trend which combines penicillin G infusions to the classical supportive measures was applied to 33 cases of severe A. phalloides poisoning, with 100% survival rates. The possible mechanism of the protective effect of penicillin G in A. phalloides poisoning is discussed.

Adult↗
PubMed1975

Studies on the 14C-histamine release induced by noradrenaline in mouse neoplastic mast cells.

Murine neoplastic mast cells incubated with labelled histamine released 14C-histamine when exposed to increasing concentrations of noradrenaline. This process was blocked by low temperature, by inhibiting oxidative metabolism and glycolysis, by calcium deprivation and by cytochalasin B. Electron microscope observations of cells exposed to noradrenaline revealed an increase of the Juxtanuclear Golgi Apparatus, and the appearance of a pronounced peripheral vacuolization. Cells exposed simultaneously to noradrenaline and cytochalasin B were characterized by a further increase of the Golgi apparatus, and by the appearance of many electron dense cytoplasmic granules. The possible mechanisms of the noradrenaline induced histamine release were discussed.

Animals↗
PubMed1975

Interaction of histamine H1-and H2-receptor antagonists with histamine uptake and metabolism by guinea-pig isolated atrium and mouse neoplastic mast cells cells in vitro.

1. Burimamide, metiamide, chlorpheniramine, triprolidine and cocaine, were tested as inhibitors of histamine uptake and metabolism in the guinea-pig atrium and in mouse neoplastic mast cells. 2. Cocaine did not affect the uptake and metabolism of histamine, either in the atrium or in the mast cells. All the antihistamines tested blocked the uptake and metabolism of histamine in both preparations. The order of potency was burimamide greater than chlorpheniramine greater than triprolidine greater than metiamide in the atrium; and burimamide greater than metiamide greater than triprolidine greater than chlorpheniramine, in the mase cells. 3. Comparison of the present results with the antihistamine activity of these blocking agents suggests that no correlation exists between the receptor blocking activity and the ability of these substances to act as inhibitors of histamine uptake and metabolism.

Animals↗
PubMedDate not supplied

Platelet aggregation and histamine release by immunological stimuli.

Platelet aggregation and histamine release were evaluated in normal and IgE pretreated human platelets exposed in vitro to IgE, anti-IgE and thrombin. The response of platelets from atopic donors directly stimulated with anti-IgE was also evaluated. Histamine release was measured by fluorimetric analysis of histamine content in platelets and in supernatants. The morphology of platelets exposed to immunological and non-immunological stimuli was recorded using an electron microscope. A detectable amount of histamine was measured in quiescent platelets. Their exposure to varying concentrations of thrombin produces a progressive aggregation which runs parallel to histamine release. The effects were significantly enhanced in platelets pretreated with IgE. Incubation of normal platelets with increasing concentrations of IgE myeloma protein, or with anti-human IgE antibody was ineffective on both aggregation and histamine release. However, incubation of platelets passively sensitized with IgE-myeloma protein with different concentrations of anti-human IgE antibody produces a concentration-dependent increase both in aggregation and histamine release. The same effects were obtained using platelets from atopic donors directly stimulated with anti-IgE. The electron microscopic pattern of platelet aggregation induced by thrombin was indistinguishable from that evoked by anti-IgE in IgE pretreated platelets. Loratadine, a non-sedative H1-receptor blocker, significantly abated platelet aggregation and histamine release induced by anti-IgE in IgE pretreated platelets.

Blood Platelets↗
PubMedDate not supplied

Cyclooxygenase-2 pathway correlates with VEGF expression in head and neck cancer. Implications for tumor angiogenesis and metastasis.

We evaluated the role of COX-2 pathway in 35 head and neck cancers (HNCs) by analyzing COX-2 expression and prostaglandin E2 (PGE2) production in relation to tumor angiogenesis and lymph node metastasis. COX-2 activity was also correlated to vascular endothelial growth factor (VEGF) mRNA and protein expression. COX-2 mRNA and protein expression was higher in tumor samples than in normal mucosa. PGE2 levels were higher in the tumor front zone in comparison with tumor core and normal mucosa (P<.0001). Specimens from patients with lymph node metastasis exhibited higher COX-2 protein expression (P=.0074), PGE2 levels (P=.0011) and microvessel density (P<.0001) than specimens from patients without metastasis. A significant correlation between COX-2 and tumor vascularization (r(s)=0.450, P=.007) as well as between COX-2 and microvessel density with VEGF expression in tumor tissues was found (r(s)=0.450, P=.007; r(s)=0.620, P=.0001, respectively). The induction of COX-2 mRNA and PGE2 synthesis by EGF and Escherichia coli lipopolysaccharide (LPS) in A-431 and SCC-9 cell lines, resulted in an increase in VEGF mRNA and protein production. Indomethacin and celecoxib reversed the EGF- and LPS-dependent COX-2, VEGF, and PGE2 increases. This study suggests a central role of COX-2 pathway in HNC angiogenesis by modulating VEGF production and indicates that COX-2 inhibitors may be useful in HNC treatment.

Aged↗
PubMedDate not supplied

Changes in the production of nitric oxide and superoxide by inflammatory cells in liver cirrhosis.

Superoxide (O2-) and nitric oxide (NO) production by polymorphonuclear leukocyte (PMNs) and monocytes in patients with liver cirrhosis were evaluated. PMNs obtained from cirrhotic patients were less effective than those from controls in producing O2- after stimulation with opsonized zymosan, while they were more effective in producing NO, as shown by the inhibition of platelet aggregation and by the increase in cGMP content. NO synthase activity was higher in leukocytes from cirrhotic patients than in controls. A correlation was found between the cardiac index and the observed changes in the inflammatory cells.

Arginine↗